Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Receptor

The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identi...

Full description

Saved in:
Bibliographic Details
Published in:Cell Vol. 168; no. 1-2; pp. 224 - 238.e10
Main Authors: Wei, Yongjie, Chiang, Wei-Chung, Sumpter, Jr, Rhea, Mishra, Prashant, Levine, Beth
Format: Journal Article
Language:English
Published: United States 12.01.2017
Subjects:
Aging - metabolism
Animals
Autophagosomes - metabolism
Caenorhabditis elegans - metabolism
Caenorhabditis elegans Proteins - metabolism
Embryo, Nonmammalian - metabolism
Membrane Proteins - metabolism
Mitochondrial Membranes - metabolism
Repressor Proteins - metabolism
mitophagy
prohibitin 2
autophagy
ISSN:1097-4172
Online Access:Get more information
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identify the inner mitochondrial membrane protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria for autophagic degradation. PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans. Our findings pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 that may underlie its roles in physiology, aging, and disease.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1097-4172
DOI:10.1016/j.cell.2016.11.042